Ask about this productRelated genes to: IL33 protein
- Gene:
- IL1RL1 NIH gene
- Name:
- interleukin 1 receptor like 1
- Previous symbol:
- -
- Synonyms:
- ST2, FIT-1, ST2L, ST2V, DER4, T1, IL33R
- Chromosome:
- 2q12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-17
- Date modifiied:
- 2017-07-07
- Gene:
- IL33 NIH gene
- Name:
- interleukin 33
- Previous symbol:
- C9orf26
- Synonyms:
- DVS27, DKFZp586H0523, NF-HEV, IL1F11
- Chromosome:
- 9p24.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-18
- Date modifiied:
- 2014-11-19
Related products to: IL33 protein
Related articles to: IL33 protein
- Information is missing on the tissue cell expression patterns of interleukin IL-33 (IL-33) and splice variants of the IL-33 receptor ST2 in normal and COPD lungs. - Source: PubMed
Publication date: 2026/03/23
Andersson Cecilia KSiddhuraj PremkumarJönsson JimmieAhlgren JohanLindö CarolineNys Josquin AScott Ian CLindstedt SandraKolbeck RolandHumbles Alison ALutter RenéSabogal Piñeros Y SJonkers René ETufvesson EllenSandén CarolineCohen E SuzanneErjefält Jonas S - Depression remains a leading cause of global disability, yet its precise neurobiological underpinnings are incompletely understood. While inflammatory cytokines have been implicated in depressive pathology, the specific role of Interleukin-33 (IL-33) and its receptor ST2 in modulating microglial-mediated neuroinflammation has remained elusive. In this study, we reveal that deficiency of the IL-33/ST2 signaling axis in naive adult male mice selectively induces depression-like behaviors without impairing memory, motor coordination, or balance. This behavioral phenotype is mechanistically linked to heightened microglial activation, increased branching complexity, and exacerbated neuronal loss within the medial prefrontal cortex (mPFC) and dentate gyrus (DG). Furthermore, we demonstrate that IL-33 counteract LPS-induced microglial activation, nuclear translocation, and subsequent neuroinflammatory responses in vitro. Collectively, these findings delineate a novel neuroimmune pathway wherein IL-33/ST2 deficiency precipitates microglia-driven neuroinflammation, thereby contributing to depressive phenotypes. - Source: PubMed
Publication date: 2026/04/28
Wang HaoyuYang SiyuDai JiapeiZheng FangLuo YiZhao JiachenDu ELei KeLei JiawenLiu JinpengXiao YifanChen HuoyingSun Yan - Intrauterine adhesion (IUA) is a common complication following endometrial injury, characterized by endometrial fibrosis and partial or complete obliteration of the uterine cavity, severely affecting menstrual function and fertility in women of reproductive age. Recent studies have demonstrated that aberrant repair processes after endometrial injury involve complex inflammatory responses and immune regulation, among which macrophage polarisation imbalance plays a critical role in fibrosis progression. As a member of the IL-1 family, IL-33 can activate the MAPK signalling pathway through binding to its receptor ST2, participating in the regulation of macrophage polarisation; however, its specific mechanisms in the pathogenesis and progression of IUA remain unclear. This study aimed to investigate the mechanism by which the IL-33/ST2/MAPK signalling pathway contributes to endometrial fibrosis following endometrial injury, and to elucidate the molecular basis through which it promotes intrauterine adhesion (IUA) formation by regulating macrophage polarisation, thereby offering a potential target for clinical intervention. - Source: PubMed
Publication date: 2026/04/26
Li GuangfengXu FengjuanLuo SangJin YiranYuan LiweiYang XitangXuan TingtingLiu Dan - The polarization of naive CD4+ T cells into Th2 cells is initiated in lymphoid organs and completed as the cells become tissue resident, where they express ST2, the receptor for the alarmin interleukin (IL)-33, which may be a key signal for tissue integration. Cellular metabolic requirements associated with this transition remain poorly understood. To address this, we compared the response of lymphoid tissue (LT) Th2 cells from helminth parasite-infected mice to stimulation by IL-33 versus through the T cell receptor via anti-CD3/CD28. We found that IL-33, but not anti-CD3/CD28, induced the development of tissue-resident like Th2 cells expressing ST2. This was associated with IL-33 induced changes in arginine metabolism linked to mTORC1 activation and polyamine synthesis, which were required for the development of tissue-resident like Th2 cells. Furthermore, IL-33 induced transcriptional changes in genes involved in chemotaxis and cell adhesion that may be critical for tissue integration. Our findings provide insights into adaptations of Th2 cells responding to tissue-integration cues and more broadly support the view that IL-33 promotes the expression of the transcriptional program associated with tissue residency of GATA3-expressing cells in adipose and possibly other tissues. - Source: PubMed
Kania Anna KSanin David EGu XinyueGidley MiaKokosinski ErykSmith AllenPearce ErikaPearce Edward J - This study aimed to examine the role of the interleukin-33 (IL-33)/suppression of tumorigenicity 2 (ST-2) signaling pathway in hepatic fibrogenesis within the microenvironment of alveolar echinococcosis (AE). The therapeutic efficacy and immunomodulatory effects of concurrent IL-33/ST-2 pathway inhibition and albendazole (ABZ) treatment were also evaluated. - Source: PubMed
Publication date: 2026/04/03
Cheng Shi-LeiMa Xiu-MeiWu Bin-JieYang Yu-XuanFan Hai-Ning